Ординатура / Офтальмология / Английские материалы / Glaucoma Medical Therapy Principles and Management_Netland_2008

218 Glaucoma Medical Therapy

Figure 12.2. (A) Ultrasound biomicrograph of anterior chamber angle in bright illumination. The iris is slightly convex, consistent with relative pupillary block. Aqueous has access to the trabecular meshwork, which is between Schwalbe’s line and the scleral spur.

(B) In the dark, the pupil dilates and the peripheral iris moves against the trabecular meshwork, closing the angle. Reprinted with permission from Ritch R, Lowe RF. Angleclosure glaucoma: mechanisms and epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis, MO: CV Mosby Co; 1996:801–819.

Glycerol is administered as a liquid in dosages of 1 to 1.5 g/kg of body weight,3 either as a 100% solution mixed with an equal volume of iced juice or as a commercial preparation (Osmoglyn, 50% solution). Oral glycerol is rapidly absorbed, is distributed throughout the extracellular water, and penetrates the eye poorly. The drug is metabolized by the liver rather than excreted by the kidneys, producing less diuresis than do other hyperosmotic agents. Glycerol has an unpleasantly sweet taste and may cause vomiting. The caloric content is 4.32 cal/g, which, combined with the osmotic diuretic effect and resultant dehydration, mandates special caution when used in diabetic patients, who may develop hyperglycemia and ketosis.4

Isosorbide (Ismotic) is more palatable, causes less nausea and vomiting, and is not metabolized—a particular advantage in diabetic patients. Although isosorbide had advantages over other osmotic drugs (see chapter 8), this drug is not commercially available at this time. A solution of 20% mannitol (Osmitrol), 0.5 to 2 g/kg, given intravenously over 45 minutes, has a greater hypotensive effect and may be given when severe nausea and vomiting are present.

Administration of hyperosmotic agents is commonly accompanied by thirst and headache. Hyperosmolar coma can be a serious complication caused by severe dehydration of the central nervous system. Patients with renal or cardiovascular disease or those already dehydrated by vomiting are at risk. These agents should be used cautiously in patients with reduced cardiac function, because the sudden intravascular volume overload may lead to congestive heart failure and pulmonary edema.5

Acetazolamide (Ak-Zol, Dazamide, Diamox), a carbonic anhydrase inhibitor (CAI), is highly effective in AAC, even in the presence of ischemic iris atrophy and paralysis of the pupil. Rapid IOP reduction is most reliably achieved by giving 500mg intravenously. Adverse reactions are uncommon. Acetazolamide tablets may be given orally as an alternative, but the onset of action is not as rapid. Following oral therapy, the maximum effect occurs at 2 hours, and high plasma levels persist for 4 to 6 hours but then drop rapidly because of excretion in the urine. Topical

aqueous suppressants are additive with acetazolamide but take longer to act, and their absorption through the cornea is slowed by corneal edema and markedly elevated IOP. They should be used in conjunction with, but not as an alternative to, systemic medications. These topical agents are more useful in later stages of treatment and in maintaining reduced IOP prior to laser iridotomy.

The liberal use of miotics to constrict the pupil and pull the peripheral iris away from the angle wall was long the main approach to AAC. A typical recommended regimen was pilocarpine 4% every 5 minutes for four doses, every 15 minutes for four doses, then every hour for four doses or until the attack was broken. However, when IOP is extremely high, the pupil is unresponsive to miotics because of ischemia and paralysis of the iris sphincter. Pilocarpine not only may be ineffective but, in some eyes, may paradoxically worsen the situation, triggering aqueous misdirection.6 Although the miotic effect of pilocarpine is blocked, ciliary muscle contraction causes thickening of the lens and forward lens movement, which results in further shallowing of the anterior chamber. For this reason, some clinicians use lower concentrations of pilocarpine (1% or 2%) with less frequent dosing. In eyes with level 3 block (phacomorphic glaucoma) or level 4 block (aqueous misdirection), pilocarpine treatment should be considered contraindicated. Unequal anterior chamber depths, progressive increase in myopia, and progressive shallowing of the anterior chamber are clues to the correct diagnosis.

High doses of pilocarpine may produce cholinergic toxicity, which may not be noticed because of the nausea and vomiting associated with the AAC glaucoma attack. Strong miotics, such as echothiophate (Phospholine Iodide), can increase both the pupillary block and the vascular congestion. Immediate treatment with intravenous acetazolamide and repeated instillation of pilocarpine 2% was not more successful in breaking attacks of AAC glaucoma than was treatment with acetazolamide and a single drop of pilocarpine given 3 hours later.7 Similar results were obtained with topically administered timolol (Blocadren) in place of acetazolamide.8

Our preferred approach to the treatment of AAC is designed to prioritize reopening of the anterior chamber angle and to minimize the possibility of adverse responses to pilocarpine.9 Examination of the affected eye and fellow eye, with attention to central and peripheral anterior chamber depth as well as the shape of the peripheral iris, is performed in an attempt to determine the underlying mechanisms of the angle closure (pupillary block, plateau iris, phacomorphic glaucoma, or aqueous misdirection). A detailed analysis of these mechanisms has been published elsewhere.1

In the absence of oral isosorbide, we use glycerol as our preferred hyperosmotic agent, along with one or more topical aqueous suppressants. Intravenous acetazolamide can be given according to the physician’s preference. The patient is then placed supine to permit the lens to fall posteriorly with vitreous dehydration. The eye is reassessed after 1 hour. IOP is usually decreased, but the angle may remains appositionally closed. One drop of pilocarpine 4% is given and the patient is reexamined 30 minutes later. If IOP is reduced and the angle is open, the patient may be treated medically with topical low-dose pilocarpine, aqueous suppressants, and corticosteroids, until the eye quiets and laser iridotomy may be performed. However, if IOP is unchanged or elevated and the angle remains closed, lens-related

220 Glaucoma Medical Therapy

angle closure should be suspected, further pilocarpine is withheld, and the attack is broken by argon laser peripheral iridoplasty (ALPI).10,11

AAC is associated with a marked inflammatory reaction. The instillation of prednisolone 1% or dexamethasone 0.1% is desirable from the start to reduce inflammation. Severe pain may be treated with analgesics, and vomiting with antiemetics.

Laser iridotomy is the procedure of choice for all cases of AAC with a component of pupillary block. Success requires gonioscopic confirmation of angle opening, because transient lowering of IOP may occur with medical therapy. Ideally, iridotomy should be performed after the acute attack has been terminated and the eye is no longer inflamed. Attacks of AAC that are unresponsive to medical treatment are almost always successfully broken with ALPI. Alternatively, ALPI with or without systemic medications may be used as immediate initial treatment, especially in eyes at risk for developing chronic angle-closure glaucoma, or eyes in which a dominant mechanism exists that is not pupillary block. It is highly effective in breaking the initial attack.12–15 In the absence of oral isosorbide and our current disinclination to use intravenous acetazolamide, we have moved to performing ALPI as an initial procedure.

ALPI does not eliminate pupillary block and is not a substitute for laser iridotomy, which must be performed as soon as the eye is quiet. However, even in eyes with extensive PAS, IOP is lowered sufficiently for a few days for the inflammation to resolve. ALPI is much safer than attempting surgical iridectomy on an inflamed eye with elevated IOP. The risks of intraoperative surgery are avoided and, even if aqueous misdirection is present, the angle remains open long enough for inflammation to clear. The alternative of waiting and prolonging medical therapy for several days seriously increases the possibility of irreversible damage to the iris, lens, drainage pathways, and optic nerve head.

12.1.2 Chronic Angle Closure. Chronic angle-closure (CAC) refers to an eye in which portions of the anterior chamber angle are permanently closed by PAS. In the era of surgical iridectomy, an attack of AAC could arise in an eye that had developed PAS because of gradual angle closure prior to the development of the attack. Conversely, a prolonged acute attack or a series of subacute attacks could lead to progressive PAS formation. The presence of PAS defined ‘‘chronic.’’ At present, we prefer the term ‘‘combined-mechanism glaucoma’’ for those eyes that have had angle closure eliminated by laser treatment and have residual elevated IOP, reserving the term ‘‘chronic angle-closure glaucoma’’ for those eyes that develop gradual sealing of the angle with PAS and gradual elevation of IOP in the absence of an acute attack.

It is important to recognize early stages of appositional angle closure in the absence of PAS and to recognize circumferential (creeping) angle closure. Laser iridotomy is indicated for all stages of CAC, opening areas of the angle not involved by PAS and preventing further synechial closure.

Prolonged miotic treatment in eyes with open-angle glaucoma and narrow angles may lead to pupillary block and angle-closure glaucoma. Zonular relaxation leads to anterior lens movement and increased lens thickness in combination with increased

pupillary block produced by pilocarpine. When miotic-induced angle closure occurs, the approach to treatment should be determined by assessing the medications necessary to control the glaucoma. If the patient has been treated with miotics alone, substitution of aqueous suppressants may suffice. If the patient requires miotics for IOP control, then laser iridotomy is warranted.

If the angle remains appositionally closed or spontaneously occludable after laser iridotomy, mechanisms other than pupillary block are likely responsible and ALPI is indicated to prevent progressive damage to, or further appositional and/or synechial closure of, the angle. The need for continued medical treatment after iridotomy with or without ALPI is determined by the level of IOP and the extent of glaucomatous damage. Treatment is similar to that of open-angle glaucoma. In two trials, lata-

noprost lowered IOP more effectively than did timolol in patients with CAC glau- coma.16–18 Latanoprost was also effective in eyes with circumferential PAS to the

level of the trabecular meshwork.19 Periodic gonioscopy is obviously warranted. Argon laser trabeculoplasty has been reported to be both successful20 and unsuccessful21 after iridotomy in combined-mechanism glaucoma. It remains to be evaluated whether selective laser trabeculoplasty is effective in this situation. If IOP remains uncontrolled and glaucomatous damage develops, filtration surgery is indicated. Patients who already present with glaucomatous optic neuropathy are unlikely to be adequately treated with iridotomy only and have a moderate chance to require filtration surgery. There is an increased chance of developing aqueous misdirection following filtration surgery in patients who have had angle-closure glaucoma.22

12.2 DISCRETE OPEN-ANGLE GLAUCOMAS

The term ‘‘primary open-angle glaucoma’’ refers to a condition characterized by elevated IOP and characteristic optic disk and/or visual field damage with no other identifiable cause at slit-lamp examination. However, the use of the word ‘‘primary’’ is suggestive of a single, discrete entity with a specific mechanism of disease causation. More likely, this category represents an assortment of disorders, as we are now seeing with the discovery of multiple genetic loci. Similarly, the term ‘‘normaltension glaucoma’’ (or ‘‘low-tension glaucoma’’) has been used to define a group of patients with glaucomatous damage but IOP less than some arbitrarily defined number. This is an artificial distinction based on population statistics. Interpretation of this term as previously used in the literature is further complicated by the recent realization that Goldmann tonometry is influenced by corneal thickness, a factor not routinely measured previously. The term ‘‘idiopathic open-angle glaucoma,’’ which reflects the present state of ignorance about the cause of the disease, would be more appropriate. As specific causes are discovered and named, the pool of idiopathic glaucoma patients will gradually decrease in size.

The concept of primary and secondary glaucomas is more a reflection of incomplete understanding regarding the pathophysiologic events that ultimately lead to glaucomatous optic atrophy and visual field loss than of any true division of the

222 Glaucoma Medical Therapy

glaucomas into primary and secondary forms.23 The term ‘‘discrete glaucomas’’ is used here to refer to well-defined entities for which there is a better understanding of causation and associated ocular findings. In the past, treatment of these glaucomas has been virtually identical to that of idiopathic (primary) open-angle glaucoma. This singularity of treatment was unfortunate, because it reduced the emphasis on accurate diagnosis and delayed the development of disease-specific treatment modalities. The sections that follow emphasize the differences in treatment of discrete glaucomas from that of idiopathic open-angle glaucoma. Some of these differences are inferential, based on logic and empirical findings, and have yet to be proven in clinical trials.

12.2.1 Pigmentary Glaucoma. Pigment dispersion syndrome (PDS) and pigmentary glaucoma (PG) are characterized by disruption of the iris pigment epithelium (IPE) and deposition of the dispersed pigment granules throughout the anterior segment. The classic diagnostic triad consists of

1.Corneal pigmentation (Krukenberg spindle)

2.Slitlike, radial, midperipheral iris transillumination defects

3.Dense trabecular pigmentation

The iris insertion is typically posterior, and the peripheral iris tends to have a concave configuration. The extent of iridolenticular contact is greater than normal, inhibiting aqueous equilibration between the posterior and the anterior chamber by preventing retrograde aqueous flow. Inhibition of blinking allows buildup of the aqueous in the posterior chamber. The act of blinking provides a mechanical pump to push aqueous from the posterior chamber to the anterior chamber.24 Once in the anterior chamber, the increased aqueous volume or pressure pushes the iris backward, accentuating the concavity—a phenomenon termed reverse pupillary block.25 Accommodation also increases the iris concavity (figure 12.3A).26–28 Iris pigment is released by mechanical damage to the IPE due to friction between the posteriorly bowed iris and the anterior zonular bundles.

Treatment may be directed at lowering IOP or stopping the basic disease process. We do not generally treat normotensive patients. If IOP is elevated and pigment is noted in the anterior chamber either spontaneously or after dilation, then treatment is initiated. A case may be made for treating younger patients with high-normal IOP, but no prospective clinical trial of medical therapy or laser iridotomy has yet been performed.

Miotic therapy reverses the iris concavity and produces a convex configuration, completely eliminating iridozonular contact (figure 12.3B). By so doing, miotics may prevent further pigment liberation and the development or progression of trabecular damage and glaucoma by immobilizing the pupil and may allow existing damage to reverse more readily. Most patients requiring therapy for PG are between the ages of 20 and 45 years and tolerate miotic drops or gel poorly because of intolerable accommodative spasm, induced myopia, and blurred vision. Pilocarpine Ocuserts, which provided low-dose pilocarpine release at a constant rate and were well tolerated, are no longer manufactured.

Figure 12.3. (A) Iris concavity in pigment dispersion syndrome. (B) Pilocarpine produces convex configuration. (C) Laser iridotomy produces planar configuration.

There is approximately a 7% incidence of retinal detachment in patients with PDS, irrespective of the presence or absence of glaucoma and of miotic treatment.29 Approximately 80% of patients with PDS are myopic. The incidence of lattice degeneration and full-thickness retinal breaks appears to be more common in eyes with PDS or PG than in the unaffected population, when the degree of myopia is compared.30 Before a miotic is prescribed for these patients, a thorough peripheral retinal examination should be performed and any retinal breaks or vitreous traction should be treated prophylactically.

In the absence of pilocarpine Ocuserts, we advocate treating patients with PDS and elevated IOP with prostaglandin analogs, to which this disease responds extremely well. Aqueous suppressants may lead to greater iridozonular contact by decreasing the volume of the posterior chamber, while decreased aqueous flow through the trabecular meshwork may allow greater blockage and dysfunction of the meshwork over the long term.31 In one short-term study, latanoprost was shown to lower IOP more effectively than timolol in patients with PG.32 It has also been

noted that PDS seems to respond to epinephrine or dipivefrin with a greater mean drop in IOP than does any other glaucoma.29,33,34

Elimination of iridozonular contact and improvement of aqueous outflow rather than inhibition of its production are more desirable in preventing glaucomatous damage by reversing the pathophysiology of the disease. Laser iridotomy relieves reverse pupillary block by allowing aqueous to flow from the anterior to the posterior chamber and produces a planar iris configuration (figure 12.3C). Whereas

224 Glaucoma Medical Therapy

pilocarpine completely inhibits exercise-induced pigment release and IOP elevation, iridotomy does so incompletely.35,36

If patients with PDS could be identified before they develop irreversible outflow obstruction, IOP elevation might be prevented with a prophylactic iridotomy. Before this treatment strategy can be recommended, however, diagnostic measures are needed to predict which patients with PDS have a sufficient risk of developing IOP elevation to justify the prophylactic iridotomy, and large, long-term trials are needed to prove that the iridotomy will prevent the eventual elevation of IOP. In a retrospective multicenter case series of 60 patients observed for a mean of 70.3 26.0 months after iridotomy in one eye, no long-term benefit was observed.37 Because the purpose of iridotomy is to prevent further pigment liberation from the iris, patients should still be in the pigment liberation stage (younger than *45 years of age). If pigment is liberated into the anterior chamber with pupillary dilation, it is suggestive that the patient is still in this stage. Patients with uncontrolled glaucoma who are facing surgery are also poor candidates, because years may be necessary to achieve functional reconstitution of the meshwork. At present, we restrict iridotomy to patients who have elevated IOP with no damage or with early glaucomatous damage.

12.2.2Exfoliation Syndrome. Glaucoma associated with exfoliation syndrome tends to respond less well to medical therapy than does idiopathic open-angle glaucoma, is more difficult to treat, is more likely to require surgical intervention, and has a worse prognosis. Patients with exfoliative glaucoma have higher IOP and more se-

vere damage at the time of detection, and their glaucomatous damage progresses more rapidly, compared with patients with primary open-angle glaucoma.38 Pa-

tients with ocular hypertension who have exfoliation syndrome are twice as likely to develop glaucoma compared with patients without exfoliation.39

Treatment of exfoliative glaucoma is usually initiated with a prostaglandin an-

alog or aqueous suppressants, similar to treatment of primary open-angle glaucoma. Latanoprost was more effective than 0.5% timolol40 and as effective as timolol– dorzolamide fixed combination41 in reducing IOP in patients with exfoliative glaucoma. On the other hand, as in PG, miotics may be a good choice of initial agent because they not only lower IOP and increase aqueous outflow but also, by inhibiting pupillary movement, decrease the amount of exfoliation material and pigment dispersed by iridolenticular contact. Miotics should enable the trabecular meshwork to clear and should slow the progression of the disease. However, many patients have nuclear sclerosis, and miotics may reduce visual acuity or dim vision sufficiently to create difficulty. Also, long-term use of miotics may lead to the development of posterior synechiae. We have found, however, that 2% pilocarpine taken at bedtime provides a nonreactive 3 mm pupil throughout the day without causing blurred vision for most patients.

Pupillary dilation in eyes with exfoliation syndrome may result in acute IOP rises accompanied by diffuse pigment dispersion in the anterior chamber.42,43

12.2.3Corticosteroid-Induced Glaucoma. Glaucoma is most commonly associated with topical application of corticosteroids, but may also result from systemic administration. Topical corticosteroid creams, lotions, or ointments placed on the eyelids,

face, or even remote sites may also be associated with IOP elevation,44,45 as may inhaled corticosteroids.46 Elevated IOP may also be produced by an increase in endogenous corticosteroids, as seen in adrenal hyperplasia or Cushing’s disease.47 Because corticosteroids may be prescribed by general physicians and because some preparations are now available over the counter, physicians and patients alike should be educated regarding their potential risks.

Patients receiving corticosteroids may develop elevated IOP from days to years after initiating treatment.48 With topical corticosteroids, IOP elevation typically occurs within 2 to 6 weeks. However, the period required and the magnitude of the IOP rise appear to depend on many factors, including the potency and dosage of the preparation, the frequency of application, the route of administration, the presence of other ocular or systemic diseases, and the individual responsiveness of the patient. In rare cases, an abrupt rise in IOP has been reported after corticosteroid administration in eyes with open angles.49

The clinical features depend on the age at presentation. In infants and very young children, corticosteroid-induced glaucoma may resemble typical findings of congenital glaucoma, with enlarged, edematous corneas.50 In older children and adults, it is clinically similar to juvenileor adult-onset idiopathic open-angle glaucoma. In patients with normal-tension glaucoma, the clinician should consider the possibility of damage from previously elevated IOP as a result of past corticosteroid use.

When corticosteroid-induced glaucoma is suspected, the agent of concern should be discontinued or used in a lower concentration. Alternatively, a weaker corticosteroid or a nonsteroidal anti-inflammatory agent (e.g., diclofenac) should be substituted. If IOP remains elevated despite discontinuation, the therapeutic approach is identical to that used for idiopathic open-angle glaucoma. If elevated IOP results from a periocular depot corticosteroid injection, excision of the depot may be necessary. IOP elevation associated with intravitreal steroid injection can be controlled with medical therapy in the large majority of cases.51 Infrequently, surgical intervention is required, in the form of vitrectomy-assisted removal of the steroid, filtration surgery, or both. Steroid-releasing implants, however, often cause marked and intractable elevation of IOP, often requiring surgical treatment. Although laser trabeculoplasty may be less effective than in eyes with other forms of glaucoma, laser treatment may be attempted prior to surgical intervention in patients more than 40 years of age.

12.2.4 Neovascular Glaucoma. Medical treatment of neovascular glaucoma can be frustrating and is often ineffective. Panretinal photocoagulation (PRP) for proliferative retinopathy should be performed. When adequate PRP is performed early, there is extensive evidence for the regression of anterior segment neovascularization in eyes with central retinal vein occlusion and proliferative diabetic retinopathy. Adjunctive medical therapy with angiogenesis-inhibiting drugs may be useful and is under evaluation at this time. Control of blood sugar is also important because near-normal glycemia is associated with later development and lesser severity of diabetic retinopathy.52

When the angle is open, medical treatment for neovascular glaucoma includes aqueous suppressants, topical corticosteroids, and a cycloplegic. Pilocarpine has been

226 Glaucoma Medical Therapy

considered relatively contraindicated because of its effect on the blood–aqueous barrier, but may be tried. Similarly, prostaglandin analogs may be tried cautiously in view of their reported association with disruption of blood–aqueous barrier and increased intraocular inflammation.

With extensive synechial angle closure, miotics are ineffective and should be considered contraindicated because of the inflammation and hyperemia they produce. Prostaglandin analogs and aqueous suppressants are beneficial but often do not lower IOP to a normal range. Hyperosmotic agents can be used intermittently. The most important medications remain topical cycloplegics and corticosteroids to decrease congestion and inflammation and prepare the eye for definitive surgery.

12.2.5 Iridocorneal Endothelial Syndrome. Patients with iridocorneal endothelial syndrome may require treatment for corneal edema, glaucoma, or both. The glaucoma can often be controlled medically in the early stages, especially with aqueous suppressants. Lowering IOP may also control the corneal edema, although the additional use of hypertonic saline solutions and soft contact lenses is often required. When medical control becomes ineffective as the disease progresses, surgical intervention is required. Argon laser trabeculoplasty is contraindicated.

12.3 TRAUMA AND GLAUCOMA

12.3.1Hyphema. Elevated IOP associated with hyphema usually responds favorably to aqueous suppressants. CAIs may also be added to the treatment regimen. However, caution is warranted with systemic acetazolamide in patients with sickle cell

hemoglobinopathy (or sickle trait), because the drug increases the concentration of ascorbic acid in the aqueous, which leads to more sickling in the anterior chamber.53 Systemic acetazolamide also causes systemic acidosis, which may exacerbate erythrocyte sickling. Methazolamide may be safer because it causes less systemic acidosis than does acetazolamide.

Surgical intervention is warranted when IOP cannot be controlled medically and threatens to cause glaucomatous damage or if corneal blood staining develops. Unfortunately, the optic disk usually cannot be visually assessed, and many patients will manifest afferent pupillary defects caused by the presence of the blood itself, rather than by the optic nerve injury. Consequently, intervention may need to be undertaken based on somewhat arbitrary criteria. Although a healthy optic nerve may be able to tolerate IOP of 40 to 50 mm Hg for 1 week or longer, a glaucomatous disk may suffer further damage with substantially lower IOP within a shorter time period. Evaluation of the fellow eye for evidence of preexisting glaucomatous optic neuropathy may thus be helpful with regard to guiding therapy.

12.3.2Angle-Recession Glaucoma. Angle-recession glaucoma usually develops years

or even decades after blunt trauma with hyphema. In one series, the mean duration between injury and diagnosis of elevated IOP was 16 years.54 In another, the time between injury and the diagnosis of glaucoma averaged 7.6 9.5 years.55 Late

glaucoma is more common if the recession involves 1808 or more of the angle. Patients with angle recession who develop glaucoma probably have a predisposition to it. The fellow eyes of patients with unilateral angle-recession glaucoma are more likely to have abnormalities of aqueous dynamics or open-angle glaucoma.

Medical therapy for angle-recession glaucoma is identical to that for idiopathic open-angle glaucoma. Pilocarpine may have little effect or a paradoxical effect on IOP. The response to medical treatment is worse, as is the response to argon laser trabeculoplasty.

12.3.3 Inflammation. Ocular inflammation is a common complication of blunt injury. In one series of 496 consecutive uveitis patients, the inflammation in 24 (4.8%) of the patients was attributed to nonpenetrating trauma.56 Trauma-induced inflammation may compromise outflow and elevate IOP by several mechanisms, including the following:

1.Obstruction of outflow pathways with inflammatory cells, debris, protein, or other serum components that are liberated because of vascular incompetence

2.Inflammation-induced swelling of the trabecular meshwork that impairs outflow

3.Inflammatory damage to trabecular endothelial cells

4.Sclerosis of the trabecular meshwork as a result of chronic inflammation

5.Obstruction of the trabecular meshwork by a hyaline membrane

Treatment with topical corticosteroids and glaucoma medications frequently affords resolution of the intraocular inflammation and IOP reduction.

Inflammation is a common complication of penetrating injury and may be associated with posterior synechiae formation, pupillary block, iris bombe, and angle-closure glaucoma. Glaucoma may result from trabecular obstruction, with inflammatory cells and debris. If there is chronic inflammation in the fellow eye, sympathetic ophthalmia should be suspected.

12.3.4Foreign Bodies. Whenever possible, foreign bodies should be removed to prevent the complications described above. Once glaucoma is present, a foreign body may be so encapsulated that standard extraction techniques may be problematic. Furthermore, the visual prognosis may already be limited by extensive retinal damage. Corticosteroids to avoid cyclitic membranes and scarring of the meshwork are also of primary importance during the early postinjury period. Antibiotics are required for endophthalmitis prophylaxis. Elevated IOP may be treated with aqueous suppressants. When medical therapy is insufficient, filtering surgery may be appropriate.

12.3.5Chemical Burns. Management of elevated IOP in the early phase of a chemical burn is limited to aqueous suppressants. However, because re-epithelialization of the ocular surface may be impaired by topical medications, systemic medications may be preferred. Miotics are relatively contraindicated, because they may aggravate anterior segment inflammation, as well as contribute to the formation of posterior